Generation of peroxynitrite and apoptosis in placenta of patients with chorioamnionitis: Possible implications in placental abruption

Mikiya Nakatsuka, Kazuo Asagiri, Yoshihiro Kimura, Yasuhiko Kamada, Katsuhiko Tada, Takafumi Kudo

Research output: Contribution to journalArticle

23 Citations (Scopus)

Abstract

The reaction of nitric oxide (NO) and superoxide results in the formation of peroxynitrite, a potent and relatively long-lived oxidant. In infectious diseases, these molecules are not only bactericidal but also toxic to host cells. Chorioamnionitis is often complicated by premature rupture of membranes and can be associated with placental abruption. These diseases are significant causes of premature low-birth-weight deliveries and consequently the morbidity and mortality of neonates. Lipopolysaccharide, bacterial endotoxin, is known to be elevated in the amniotic fluid of patients with chorioamnionitis. Lipopolysaccharide is known to induce the formation of NO and superoxide. We report here that nitrite/nitrate, stable metabolites of NO, were increased in serum from patients with chorioamnionitis. Immunohistochemical studies demonstrated enhanced expression of inducible NO synthase and formation of nitrotyrosine, a footprint of peroxynitrite, in the placentae from patients with chorioamnionitis and also in patients with placental abruption. Furthermore, apoptotic cell death was also increased in the placentae from patients with both diseases. These results suggest that chorioamnionitis and a portion of placental abruption may share a common cascade of placental injury. Nitric oxide and its metabolites may play an important role in this cascade.

Original languageEnglish
Pages (from-to)1101-1106
Number of pages6
JournalHuman Reproduction
Volume14
Issue number4
Publication statusPublished - 1999

Fingerprint

Abruptio Placentae
Chorioamnionitis
Peroxynitrous Acid
Placenta
Apoptosis
Nitric Oxide
Superoxides
Lipopolysaccharides
Poisons
Premature Birth
Low Birth Weight Infant
Nitric Oxide Synthase Type II
Amniotic Fluid
Nitrites
Oxidants
Endotoxins
Nitrates
Communicable Diseases
Rupture
Cell Death

Keywords

  • Apoptosis
  • Chorioamnionitis
  • Interleukin-1β-converting enzyme (ICE)
  • Peroxynitrite
  • Placental abruption

ASJC Scopus subject areas

  • Physiology
  • Developmental Biology
  • Obstetrics and Gynaecology
  • Reproductive Medicine

Cite this

Generation of peroxynitrite and apoptosis in placenta of patients with chorioamnionitis : Possible implications in placental abruption. / Nakatsuka, Mikiya; Asagiri, Kazuo; Kimura, Yoshihiro; Kamada, Yasuhiko; Tada, Katsuhiko; Kudo, Takafumi.

In: Human Reproduction, Vol. 14, No. 4, 1999, p. 1101-1106.

Research output: Contribution to journalArticle

@article{bf73a1315f9542ec8d8a4749b032772b,
title = "Generation of peroxynitrite and apoptosis in placenta of patients with chorioamnionitis: Possible implications in placental abruption",
abstract = "The reaction of nitric oxide (NO) and superoxide results in the formation of peroxynitrite, a potent and relatively long-lived oxidant. In infectious diseases, these molecules are not only bactericidal but also toxic to host cells. Chorioamnionitis is often complicated by premature rupture of membranes and can be associated with placental abruption. These diseases are significant causes of premature low-birth-weight deliveries and consequently the morbidity and mortality of neonates. Lipopolysaccharide, bacterial endotoxin, is known to be elevated in the amniotic fluid of patients with chorioamnionitis. Lipopolysaccharide is known to induce the formation of NO and superoxide. We report here that nitrite/nitrate, stable metabolites of NO, were increased in serum from patients with chorioamnionitis. Immunohistochemical studies demonstrated enhanced expression of inducible NO synthase and formation of nitrotyrosine, a footprint of peroxynitrite, in the placentae from patients with chorioamnionitis and also in patients with placental abruption. Furthermore, apoptotic cell death was also increased in the placentae from patients with both diseases. These results suggest that chorioamnionitis and a portion of placental abruption may share a common cascade of placental injury. Nitric oxide and its metabolites may play an important role in this cascade.",
keywords = "Apoptosis, Chorioamnionitis, Interleukin-1β-converting enzyme (ICE), Peroxynitrite, Placental abruption",
author = "Mikiya Nakatsuka and Kazuo Asagiri and Yoshihiro Kimura and Yasuhiko Kamada and Katsuhiko Tada and Takafumi Kudo",
year = "1999",
language = "English",
volume = "14",
pages = "1101--1106",
journal = "Human Reproduction",
issn = "0268-1161",
publisher = "Oxford University Press",
number = "4",

}

TY - JOUR

T1 - Generation of peroxynitrite and apoptosis in placenta of patients with chorioamnionitis

T2 - Possible implications in placental abruption

AU - Nakatsuka, Mikiya

AU - Asagiri, Kazuo

AU - Kimura, Yoshihiro

AU - Kamada, Yasuhiko

AU - Tada, Katsuhiko

AU - Kudo, Takafumi

PY - 1999

Y1 - 1999

N2 - The reaction of nitric oxide (NO) and superoxide results in the formation of peroxynitrite, a potent and relatively long-lived oxidant. In infectious diseases, these molecules are not only bactericidal but also toxic to host cells. Chorioamnionitis is often complicated by premature rupture of membranes and can be associated with placental abruption. These diseases are significant causes of premature low-birth-weight deliveries and consequently the morbidity and mortality of neonates. Lipopolysaccharide, bacterial endotoxin, is known to be elevated in the amniotic fluid of patients with chorioamnionitis. Lipopolysaccharide is known to induce the formation of NO and superoxide. We report here that nitrite/nitrate, stable metabolites of NO, were increased in serum from patients with chorioamnionitis. Immunohistochemical studies demonstrated enhanced expression of inducible NO synthase and formation of nitrotyrosine, a footprint of peroxynitrite, in the placentae from patients with chorioamnionitis and also in patients with placental abruption. Furthermore, apoptotic cell death was also increased in the placentae from patients with both diseases. These results suggest that chorioamnionitis and a portion of placental abruption may share a common cascade of placental injury. Nitric oxide and its metabolites may play an important role in this cascade.

AB - The reaction of nitric oxide (NO) and superoxide results in the formation of peroxynitrite, a potent and relatively long-lived oxidant. In infectious diseases, these molecules are not only bactericidal but also toxic to host cells. Chorioamnionitis is often complicated by premature rupture of membranes and can be associated with placental abruption. These diseases are significant causes of premature low-birth-weight deliveries and consequently the morbidity and mortality of neonates. Lipopolysaccharide, bacterial endotoxin, is known to be elevated in the amniotic fluid of patients with chorioamnionitis. Lipopolysaccharide is known to induce the formation of NO and superoxide. We report here that nitrite/nitrate, stable metabolites of NO, were increased in serum from patients with chorioamnionitis. Immunohistochemical studies demonstrated enhanced expression of inducible NO synthase and formation of nitrotyrosine, a footprint of peroxynitrite, in the placentae from patients with chorioamnionitis and also in patients with placental abruption. Furthermore, apoptotic cell death was also increased in the placentae from patients with both diseases. These results suggest that chorioamnionitis and a portion of placental abruption may share a common cascade of placental injury. Nitric oxide and its metabolites may play an important role in this cascade.

KW - Apoptosis

KW - Chorioamnionitis

KW - Interleukin-1β-converting enzyme (ICE)

KW - Peroxynitrite

KW - Placental abruption

UR - http://www.scopus.com/inward/record.url?scp=0032944357&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0032944357&partnerID=8YFLogxK

M3 - Article

C2 - 10221248

AN - SCOPUS:0032944357

VL - 14

SP - 1101

EP - 1106

JO - Human Reproduction

JF - Human Reproduction

SN - 0268-1161

IS - 4

ER -